The authors confirmed that in mice and patients with prostate cancer, abiraterone is converted to the more active Δ4-abiraterone (D4A), which inhibits CYP17A1, 3βHSD, and steroid-5α-reductase (SRD5A), required for DHT synthesis, and then antagonizes the androgen receptor, providing an additional explanation for the clinical abiraterone activity. This evidence concerns the gene AR and Familial prostate cancer.